Differential response of rat cardiac and skeletal muscle glycogen to glucocorticoids

1982 ◽  
Vol 60 (5) ◽  
pp. 634-637 ◽  
Author(s):  
James L. Poland ◽  
Jerry W. Poland ◽  
Richard N. Honey

Though glucocorticoids were previously implicated in the support of myocardial glycogen supercompensation after exercise, it was unclear why skeletal muscle glycogen did not simultaneously supercompensate since it was also exposed to the exercise-induced glucocorticoid increases. The current study shows that glucocorticoids differentially affect cardiac and skeletal muscle glycogen. Following dexamethasone administration (400 μg i.p.) myocardial glycogen peaked at 6 h while glycogen in the soleus, red vastus lateralis, and white vastus lateralis increased more slowly and reached the highest values 17 h postinjection. Concurrently, blood glucose, insulin, and glucagon remained at control levels. Liver glycogen increased within 2 h and continued to rise with a peak value at 17 h. Plasma free fatty acid (FFA) levels increased and remained high throughout the 26-h experimental period. High FFA levels inhibit glycogenolysis and thus could be partially responsible for glucocorticoid-induced glycogen increases. It is postulated that glycogen supercompensation does not readily occur in skeletal muscles after exercise because of the brevity of the corticosterone and FFA increases and the slowness of the skeletal muscle glycogen response to glucocorticoids.

1999 ◽  
Vol 77 (4) ◽  
pp. 300-304 ◽  
Author(s):  
A Ramamani ◽  
M M Aruldhas ◽  
P Govindarajulu

Although reports on sex steroids have implicated them as promoting protein synthesis and also providing extra strength to the skeletal muscle, it remains unclear whether sex steroids affect glycogen metabolism to provide energy for skeletal muscle functions, since glycogen metabolism is one of the pathways that provides energy for the skeletal muscle contraction and relaxation cycle. The purpose of the current study was to show that testosterone and estradiol act differentially on skeletal muscles from different regions, differentially with reference to glycogen metabolism. To study this hypothesis, healthy mature male Wistar rats (90-120 days of age, weighing about 180-200 g) were castrated (a bilateral orchidectomy was performed to test the significance of skeletal muscle glycogen metabolism in the absence of testosterone). One group of castrated rats was supplemented with testosterone (100 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards). To test whether estradiol has any effect on male skeletal muscle glycogen metabolism 17beta-estradiol (5 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards) was administered to orchidectomized rats. To test whether these sex steroids have any differential effect on skeletal muscles from different regions, skeletal muscles from the temporal region (temporalis), muscle of mastication (masseter), forearm muscle (triceps and biceps), thigh muscle (vastus lateralis and gracilis), and calf muscle (gastrocnemius and soleus) were considered. Castration enhanced blood glucose levels and decreased glycogen stores in skeletal muscle from head, jaw, forearm, thigh, and leg regions. This was accompanied by diminished activity of glycogen synthetase and enhanced activity of muscle phosphorylase. Following testosterone supplementation to castrated rats, a normal pattern of all these parameters was maintained. Estradiol administration to castrated rats did not bring about any significant alteration in any of the parameters. The data obtained suggest a stimulatory effect of testosterone on skeletal muscle glycogenesis and an inhibitory effect on glycogenolysis. Estradiol did not play any significant role in the skeletal muscle glycogen metabolism of male rats.Key words: testosterone, estradiol, skeletal muscle, glycogen metabolism.


1991 ◽  
Vol 71 (3) ◽  
pp. 1015-1019 ◽  
Author(s):  
M. F. Mottola ◽  
P. D. Christopher

To examine the effects of maternal exercise on liver and skeletal muscle glycogen storage, female Sprague-Dawley rats were randomly divided into control, nonpregnant runner, pregnant nonrunning control, pregnant runner, and prepregnant exercised control groups. The exercise consisted of treadmill running at 30 m/min on a 10 degree incline for 60 min, 5 days/wk. Pregnancy alone, on day 20 of gestation, decreased maternal liver glycogen content and increased red and white gastrocnemius muscle glycogen storage above control values (P less than 0.05). In contrast, exercise in nonpregnant animals augmented liver glycogen storage and also increased red and white gastrocnemius glycogen content (P less than 0.05). By combining exercise and pregnancy, the decrease in liver glycogen storage in the pregnant nonexercised condition was prevented in the pregnant runner group and more glycogen was stored in both the red and white portions of the gastrocnemius than all other groups (P less than 0.05). Fetal body weight was greatest (P less than 0.05) in the pregnant runner group and lowest (P less than 0.05) in the prepregnant exercise control group. These results demonstrate that chronic maternal exercise may change maternal glycogen storage patterns in the liver and skeletal muscle with some alteration in fetal outcome.


1974 ◽  
Vol 52 (1) ◽  
pp. 119-122 ◽  
Author(s):  
A. W. Taylor ◽  
J. Stothart ◽  
M. A. Booth ◽  
R. Thayer ◽  
S. Rao

Sixteen healthy male subjects classified as sedentary (8) or active (8), exercised to exhaustion on a bicycle ergometer at a load requiring 70% of their maximal aerobic capacity. Biopsy samples of the vastus lateralis muscle were taken at rest and at the time of fatigue. A 12 week training program increased skeletal muscle glycogen content and branching enzyme activities twofold. The exhaustive submaximal exercise reduced the glycogen levels of the trained group to values similar to the fatigue levels of the non-trained subjects. Skeletal muscle glycogen branching enzyme activities decreased with submaximal exercise to fatigue in all groups. Maximal exercise to fatigue resulted in small increases in the activities of the enzyme. The results of the present study and a previous study (Taylor et al. 1972. Can. J. Physiol. Pharmacol. 50, 411–415) indicate that the activities of the glycogen synthesizing enzymes are highly correlated with the skeletal muscle resting glycogen concentration and the relative fitness of the subjects.


2010 ◽  
Vol 299 (6) ◽  
pp. E1053-E1060 ◽  
Author(s):  
Joachim Nielsen ◽  
Charlotte Suetta ◽  
Lars G. Hvid ◽  
Henrik D. Schrøder ◽  
Per Aagaard ◽  
...  

Previous studies have shown that skeletal muscle glycogen and mitochondria are distributed in distinct subcellular localizations, but the role and regulation of these subcellular localizations are unclear. In the present study, we used transmission electron microscopy to investigate the effect of disuse and aging on human skeletal muscle glycogen and mitochondria content in subsarcolemmal (SS), intermyofibrillar (IMF), and intramyofibrillar (intra) localizations. Five young (∼23 yr) and five old (∼66 yr) recreationally active men had their quadriceps muscle immobilized for 2 wk by whole leg casting. Biopsies were obtained from m. vastus lateralis before and after the immobilization period. Immobilization induced a decrement of intra glycogen content by 54% ( P < 0.001) in both age groups and in two ultrastructurally distinct fiber types, whereas the content of IMF and SS glycogen remained unchanged. A localization-dependent decrease ( P = 0.03) in mitochondria content following immobilization was found in both age groups, where SS mitochondria decreased by 33% ( P = 0.02), superficial IMF mitochondria decreased by 20% ( P = 0.05), and central IMF mitochondria remained unchanged. In conclusion, our findings demonstrate a localization-dependent adaptation to immobilization in glycogen and mitochondria content of skeletal muscles of both young and old individuals. Specifically, this suggests that short-term disuse preferentially affects glycogen particles located inside the myofibrils and that mitochondria volume plasticity can be dependent on the distance to the fiber border.


1980 ◽  
Vol 58 (10) ◽  
pp. 1229-1233 ◽  
Author(s):  
James L. Poland ◽  
Carolyn Trowbridge ◽  
Jerry W. Poland

Carbohydrate and lipid substrates were measured in rats during recovery following exercise or a 24-h fast and compared with values from time-matched control (rested, fed) rats. After exercise muscle glycogen recovered at the expense of liver glycogen repletion. Myocardial glycogen supercompensated whereas soleus, red vastus lateralis (RVL) and white vastus lateralis glycogen merely returned to control levels. A similar recovery pattern occurred after fasting with refeeding promoting glycogen synthesis in the liver, skeletal muscles, and even in the myocardium, where glycogen had already been elevated by the fast. Both soleus and RVL muscles, along with the myocardium, exhibited glycogen supercompensation. Both exercise and fasting increased plasma free fatty acid (FFA) levels which favor myocardial glycogen synthesis. Unchanged tissue triglycerides and relatively stable blood glucose levels suggest that these are unlikely influences on glycogen recovery. It is concluded that exercise per se is unlikely to induce glycogen supercompensation in skeletal muscles though myocardial glycogen supercompensation readily occurs, that food restriction prior to exercise quantitatively affects substrate recovery though its impact could go unnoticed because of the qualitative similarities between substrate recovery following exercise or fasting, and that FFA is the only major energy substrate concurrently changing with glycogen after exercise or fasting which could facilitate glycogen synthesis.


1976 ◽  
Vol 231 (2) ◽  
pp. 614-618 ◽  
Author(s):  
RK Conlee ◽  
MJ Rennie ◽  
WW Winder

To test whether skeletal muscle glycogen concentration is related to food consumption, glycogen content was determined in red (R) and white (W) vastus lateralis and in soleus (S) muscles from six groups of ad libitum-fed rats killed at 4-h intervals and from 24-h-fasted animals killed at 0800 and 1600 h. The animal quarters were illuminated between 0700 and 1900 h. Glycogen values exhibited a peak at 0800 h and a nadir at 2000 h. These changes bore no relationship to blood glucose and lactate or plasma free fatty acids, glucagon, insulin, and corticosterone concentrations. Fasting resulted in reductions of glycogen content of 49% (S), 47% (R), and 29% (W) in animals killed at 0800h, but at 1600h changes were only 23% (RY), 17% (W), and 8% (S). The smaller changes at 1600 h were apparently due to lower glycogen levels in the tissues of the fed animals. It was concluded that skeletal muscle exhibits a diurnal variation in glycogen content, and that, contrary to accepted belief, fating significantly alters muscle glycogen concentration.


Diabetes ◽  
2009 ◽  
Vol 59 (1) ◽  
pp. 26-32 ◽  
Author(s):  
K. Kiilerich ◽  
M. Gudmundsson ◽  
J. B. Birk ◽  
C. Lundby ◽  
S. Taudorf ◽  
...  

1999 ◽  
Vol 277 (3) ◽  
pp. E544-E550 ◽  
Author(s):  
Robert M. O’Doherty ◽  
Paul R. Anderson ◽  
Allan Z. Zhao ◽  
Karin E. Bornfeldt ◽  
Christopher B. Newgard

The effect of moderate hyperleptinemia (∼20 ng/ml) on liver and skeletal muscle glycogen metabolism was examined in Wistar rats. Animals were studied ∼90 h after receiving recombinant adenoviruses encoding rat leptin (AdCMV-leptin) or β-galactosidase (AdCMV-βGal). Liver and skeletal muscle glycogen levels in the fed and fasted (18 h) states were similar in AdCMV-leptin- and AdCMV-βGal-treated rats. However, after delivery of a glucose bolus, liver glycogen levels were significantly greater in AdCMV-leptin compared with AdCMV-βGal rats ( P < 0.05). To investigate the mechanism(s) of these differences, glycogen levels were measured immediately after the cessation of a 3- or 6-h glucose infusion or 3, 6, and 9 h after the cessation of a 6-h glucose infusion. Similar increases in liver and skeletal muscle glycogen occurred in hyperleptinemic and control rats in response to glucose infusions. However, 3 and 6 h after the cessation of a glucose infusion, liver glycogen levels were approximately twofold greater ( P < 0.05) in AdCMV-leptin-treated compared with AdCMV-βGal-treated animals. Skeletal muscle glycogen levels were similar in AdCMV-leptin-treated and AdCMV-βGal-treated animals at the same time points. Glycogen phosphorylase, phosphodiesterase 3B, and glycogen synthase activities were unaltered by hyperleptinemia. We conclude that moderate increases in plasma leptin levels decrease liver glycogen degradation during the fed-to-fasted transition.


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